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前列环素(PGI2)可抑制人类血小板中由二磷酸腺苷(ADP)和花生四烯酸诱导的形态变化及促凝血活性的发展。

Prostacyclin (PGI2) inhibits the development in human platelets of ADP and arachidonic acid-induced shape change and procoagulant activity.

作者信息

Ehrman M L, Jaffe E A

出版信息

Prostaglandins. 1980 Dec;20(6):1103-16. doi: 10.1016/0090-6980(80)90063-5.

Abstract

Platelets which change shape from discs to spheres concomitantly develop platelet procoagulant activity which is independent of and precedes aggregation or the release reaction. Since prostacyclin (PGI2) is known to be a potent inhibitor of platelet aggregation and release, the effect of PGI2 on platelet shape change and the development of platelet procoagulant activity was measured. Platelet shape change (percent discs and spheres) was assayed by a light transmission technique. Platelet procoagulant activity was assayed using recalcified clotting times measured concurrently (by aggregometry) with platelet shape assays. PGI2 inhibited the development of platelet shape change and procoagulant activity induced by the addition of ADP (0.7 microM); the 50% inhibitory dose of PGI2 was approximately 2 nM. PGI2 also inhibited arachidonic acid (0.3-1.2 mM) induced platelet shape change and procoagulant activity; the 50% inhibitory dose of PGI2 was 2.3 nM. Thus, physiologic concentrations of PGI2 inhibit platelet shape change and prevent the development of sphering associated procoagulant activity.

摘要

血小板从圆盘状转变为球状的同时会产生血小板促凝活性,这种活性独立于聚集或释放反应且先于它们出现。由于已知前列环素(PGI2)是血小板聚集和释放的强效抑制剂,因此测定了PGI2对血小板形状变化和血小板促凝活性发展的影响。血小板形状变化(圆盘状和球状的百分比)通过光透射技术进行测定。血小板促凝活性通过与血小板形状测定同时(通过凝集测定法)测量的复钙凝血时间来测定。PGI2抑制由添加ADP(0.7微摩尔)诱导的血小板形状变化和促凝活性;PGI2的50%抑制剂量约为2纳摩尔。PGI2还抑制花生四烯酸(0.3 - 1.2毫摩尔)诱导的血小板形状变化和促凝活性;PGI2的50%抑制剂量为2.3纳摩尔。因此,生理浓度的PGI2抑制血小板形状变化并阻止与球状相关的促凝活性的发展。

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